Assessment of dynamic cardiac repolarization and contractility in patients with hypertrophic cardiomyopathy.

Aims: Arrhythmia mechanisms in hypertrophic cardiomyopathy remain uncertain. Preclinical models suggest hypertrophic cardiomyopathy-linked mutations perturb sarcomere length-dependent activation, alter cardiac repolarization in rate-dependent fashion and potentiate triggered electrical activity. This study was designed to assess rate-dependence of clinical surrogates of contractility and repolarization in humans with hypertrophic cardiomyopathy.

Premature battery depletion due to compromised low-voltage capacitor in a family of defibrillators.

Background: Boston Scientific (Marlborough, MA, USA) implantable cardioverter-defibrillators (ICDs) and cardiac resynchronization therapy defibrillators (CRT-Ds) manufactured between 2008 and 2014 are potentially subject to premature battery depletion through a low-voltage capacitor malfunction occurring as a result of hydrogen buildup within the device. Although some of these devices are currently under advisory, other devices manufactured during this timeframe carry a lower risk of the same malfunction. These same devices are known to have superior longevity in general, and the overall mean lifespan of the devices remains long.

Signal-averaged P wave area increases during respiratory events in patients with paroxysmal atrial fibrillation and obstructive sleep apnea.

Purpose: P wave characteristics change during simulated apneic events in individuals with atrial fibrillation (AF). This study sought to assess whether similar changes occur during nocturnal respiratory events in patients with AF and obstructive sleep apnea (OSA).

Methods: Thirty-five individuals with severe OSA who underwent formal polysomnography and subsequent AF ablation were compared to a matched group without AF.

Improvement in Sleep-Disordered Breathing Indices Downloaded From a Positive Airway Pressure Machine Following Conversion of Atrial Fibrillation to Sinus Rhythm.

Sleep-disordered breathing (SDB) is a contributor to atrial fibrillation (AF) and treatment of obstructive sleep apnea can reduce the recurrence of AF following catheter ablation. However, the effect of AF therapies on measures of SDB severity is less robustly described. We present the case of a middle-aged man with SDB and persistent AF who exhibited improvement in SDB metrics, as characterized by data downloaded from his auto-titrating continuous positive airway pressure (AutoCPAP) machine, very shortly following procedures that restored sinus rhythm.

Efficacy of a Bio-Absorbable Antibacterial Envelope to Prevent Cardiac Implantable Electronic Device Infections in High-Risk Subjects.

Introduction: Cardiac implantable electronic device (CIED) infections are potentially preventable complications associated with high morbidity, mortality, and cost. A recently developed bio-absorbable antibacterial envelope (TYRX™-A) might prevent CIED infections in high-risk subjects. However, data regarding safety and efficacy have not been published.

The AFFORD clinical decision aid to identify emergency department patients with atrial fibrillation at low risk for 30-day adverse events.

There is wide variation in the management of patients with atrial fibrillation (AF) in the emergency department (ED). We aimed to derive and internally validate the first prospective, ED-based clinical decision aid to identify patients with AF at low risk for 30-day adverse events. We performed a prospective cohort study at a university-affiliated tertiary-care ED.

Electrophysiologic substrate in congenital Long QT syndrome: noninvasive mapping with electrocardiographic imaging (ECGI).

Background: Congenital Long QT syndrome (LQTS) is an arrhythmogenic disorder that causes syncope and sudden death. Although its genetic basis has become well-understood, the mechanisms whereby mutations translate to arrhythmia susceptibility in the in situ human heart have not been fully defined. We used noninvasive ECG imaging to map the cardiac electrophysiological substrate and examine whether LQTS patients display regional heterogeneities in repolarization, a substrate that promotes arrhythmogenesis.

Usefulness of a low CHADS2 or CHA2DS2-VASc score to predict normal diagnostic testing in emergency department patients with an acute exacerbation of previously diagnosed atrial fibrillation.

International guidelines do not specify what testing should be performed during emergency department (ED) evaluations for patients presenting with an exacerbation of previously diagnosed atrial fibrillation (AF). We hypothesized that low CHADS2 and CHA2DS2-VASc scores predict normal routine diagnostic testing in these patients. We conducted an analysis within a prospective observational cohort study at a university-affiliated hospital.

Risk factors for bradycardia requiring pacemaker implantation in patients with atrial fibrillation.

Symptomatic bradycardia may complicate atrial fibrillation (AF) and necessitate a permanent pacemaker. Identifying patients at increased risk for symptomatic bradycardia may reduce associated morbidities and health care costs. The aim of this study was to investigate predictors for developing bradycardia requiring a permanent pacemaker in patients with AF.

Augmented potassium current is a shared phenotype for two genetic defects associated with familial atrial fibrillation.

Mutations in multiple genes have been implicated in familial atrial fibrillation (AF), but the underlying mechanisms, and thus implications for therapy, remain ill-defined. Among 231 participants in the Vanderbilt AF Registry, we found a mutation in KCNQ1 (encoding the alpha-subunit of slow delayed rectifier potassium current [I(Ks)]) and separately a mutation in natriuretic peptide precursor A (NPPA) gene (encoding atrial natriuretic peptide, ANP), both segregating with early onset lone AF in different kindreds. The functional effects of these mutations yielded strikingly similar I(Ks) "gain-of-function.

Cardiac potassium channel dysfunction in sudden infant death syndrome.

Life-threatening arrhythmias have been suspected as one cause of the sudden infant death syndrome (SIDS), and this hypothesis is supported by the observation that mutations in arrhythmia susceptibility genes occur in 5-10% of cases. However, the functional consequences of cardiac potassium channel gene mutations associated with SIDS and how these alleles might mechanistically predispose to sudden death are unknown. To address these questions, we studied four missense KCNH2 (encoding HERG) variants, one compound KCNH2 genotype, and a missense KCNQ1 mutation all previously identified in Norwegian SIDS cases.